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772 PA R T V / Health Promotion and Disease Prevention
Catecholamine and
cortisol release
Increased platelet
reactivity
Increased thrombin Ischemia
Moderate to
activity Plaque rupture
intense mental
Myocardial infarction
stress
Increased autonomic Sudden cardiac death
imbalance
Decreased heart rate
variability
Increased systolic and
diastolic blood pressure ■ Figure 33-1 Physiologic mechanisms
linking stress and coronary heart disease.
Increased oxygen use
Increased coronary
vasoconstriction
Increased macrophage
activity
Increased cytokine
activity
Increased lipid synthesis
and mobilization
the effect of depression on survival after an acute MI. Thus, treat- smoking, are likely to contribute to the development of CHD
ment that improves depression and heart rate variability can also and, unless modified following an MI, increase the susceptibility
improve survival. Those with hostile traits usually have high blood toward future events. Both of these theories may explain the link
pressure, heart rate, and neuroendocrine responses, such as corti- between psychosocial risk factors and CHD.
59
sol release, in frustrating or harassing situations. When the neg-
ative emotions of depression, anger, and anxiety were simultane-
ously evaluated in the same group of patients who suffered an MI, ASSESSMENT OF
both depression and anxiety were significant independent predic- PSYCHOSOCIAL RISK FACTORS
14
tors of subsequent cardiac events. Dividing events into throm- RELATED TO CHD
bogenic events (infarction or unstable angina) and arrhythmic
events, the authors in this study found that anxiety and a history Nurses in any practice setting are encouraged to evaluate patients
of depression were associated with thrombogenic events, while not only for the traditional risk factors but also for psychosocial
current depression and anger were associated with arrhythmic risk factors. In the following discussion of subjective and objective
events. The authors speculate that mechanisms such as enhanced assessment of depression, low-perceived social support, anxiety,
platelet adhesion leading to plaque instability and thrombosis and hostility and anger, note that several of these psychosocial risk
might account for these results. These biologic pathways have yet factors may be present concurrently.
to be tested.
Behavioral mechanism theories such as negative affective states Screening for Depression
also perpetuate behaviors such as social withdrawal, lack of pleasur-
able activities, chronic angry outbursts, and disconnection from sup- Depression has a complex variable definition, and measurement
port, which can adversely affect cardiac physiology. Also, patients can often be difficult in patients with coexisting medical prob-
99
who experience psychosocial risk factors may be less compliant with lems. 98 Jiang et al. have questioned the sensitivity of the screen-
risk-reduction strategies, and their noncompliant behaviors may be ing instruments for depression and have highlighted the difficulty
the mechanism associated with the development of CHD and its of differentiating a normal grief response from a diagnosis of sig-
prognosis. Longstanding negative behaviors, such as a high-calorie nificant depression. Although the diagnosis of depression often re-
diet, inadequate self-care, inadequate sleep, lack of exercise, and quires the skill of a licensed mental health practitioner, nurses,

